Recent reports have suggested that the life sustaining mineralocorticoid, aldosterone, is partially bound to transcortin or, in one report, a specific aldosterone binding globulin. The metabolic clearance of aldosterone (plasma) is said to be reduced and plasma aldosterone increased in essential hypertension. Zipser and Horton' however, report that whole blood clearance is not altered by ACTH or cortisol and both plasma and whole blood hepatic extraction is nearly complete. We propose a study of aldosterone binding by both equilibrium dialysis and red cell distribution. This data in normal and hypertensive subjects will be compared with plasma and whole blood hepatic extraction in some of these patients undergoing indicated cardiac catheterization. Further characterization of adosterone binding in vitro will use displacement by other steroids and double antibody precipitation of CBG in the presence of tracer aldosterone. This work will 1) determine if there is a binding and hepatic defect in hypertensives, 2) ascertain whether all aldosterone binding to globulin is CBG, 3) suggest whether whole blood assay of aldosterone is a better reflection of in vivo events.